a. Fatty changes to the liver
b. Alcoholic hepatitis
Fatty change, or steatosis is the accumulation of fat in liver cells which can be seen as fatty globules under the microscope. Alcoholism causes large fatty globules (macrovesicular steatosis). Small fatty globules have different causes. Other causes of macrovesicular steatosis include diabetes, obesity and starvation. Alcoholic fatty change is probably dose-related. The mechanism of alcohol induced fatty liver involves an above average NADH:NAD ratio caused by alcohol metabolism by alcohol dehydrogenase and aldehyde dehydrogenase. A higher NADH concentration induces fatty acid synthesis while decreased NAD level causes decreased fatty acid oxidation. Consequently, the higher levels of fatty acid signals the hepatocytes to compound it to glycerol to form triglycerides.
Some people get an acute hepatitis or inflammatory reaction to the cells affected by fatty change. This is not directly related to the dose of alcohol. Some people seem more prone to this reaction than others. This is called alcoholic steatonecrosis and the inflammation probably predisposes to liver fibrosis.
Cirrhosis is a late stage of liver disease marked by fibrosis and altered liver architecture. It is often progressive and may eventually lead to liver failure. Late complications of cirrhosis or liver failure include portal hypertension, coagulation disorders, ascites and other complications, including hepatic encephalopathy and the hepatorenal syndrome.
Cirrhosis also has number of causes besides alcohol abuse, such as viral hepatitis and non-alcoholic toxins. The late stages of cirrhosis may look similar regardless of cause. This phenomenon is termed a "final common pathway" for the disease.
Fatty change and alcoholic hepatitis are probably reversible. The later stages of fibrosis and cirrhosis tend to be irreversible but can usually be quite well managed for long periods of time.
As the liver scars, the blood vessels become non-compliant and narrow. This leads to increased pressure in blood vessels entering the liver. Over time, this causes a back log of blood (portal hypertension) and is associated with massive bleeding. Enlarged veins also develop to bypass the blockages in the liver. These veins are very fragile and do have a tendency to rupture and bleed (varices). Variceal bleeding can be life threatening and needs emergent treatment. Once the liver is damaged, fluid builds up in the abdomen and legs. The fluid buildup presses on the diaphragm and can make breathing very difficult. As liver damage progresses, the liver is unable to get rid of pigments like bilirubin and both the skin and eyes turn yellow. The dark pigment also causes the urine to appear dark and the stools appear pale. Also with the progression of the disease, the liver can release toxic substances (ammonia) which then lead to brain damage. This results in altered mental status, behavior and personality changes.
Not brilliant really...
Possession of a class A drug with intent to supply has a maximum sentencing tariff of life imprisonment. Possession for own use 2 - 6 years imprisonment usually. Either way it would seriously screw up a young life, permanently!